Gamow-Jordan Vectors and Non-Reducible Density Operators from Higher Order S-Matrix Poles

In analogy to Gamow vectors that are obtained from first order resonance poles of the S-matrix, one can also define higher order Gamow vectors which are derived from higher order poles of the S-matrix. An S-matrix pole of r-th order at z_R=E_R-i\Gamma/2 leads to r generalized eigenvectors of order k= 0, 1, ... , r-1, which are also Jordan vectors of degree (k+1) with generalized eigenvalue (E_R-i\Gamma/2). The Gamow-Jordan vectors are elements of a generalized complex eigenvector expansion, whose form suggests the definition of a state operator (density matrix) for the microphysical decaying state of this higher order pole. This microphysical state is a mixture of non-reducible components. In spite of the fact that the k-th order Gamow-Jordan vectors has the polynomial time-dependence which one always associates with higher order poles, the microphysical state obeys a purely exponential decay law.Comment: 39 pages, 3 PostScript figures; sub2.eps may stall some printers and should then be printed out separately; ghostview is o.

Sex differences in genetic mechanisms for mammalian brain and behavior

There are sex specific genetic mechanisms for mammalian brain and behavior. These are genes that act differently in each sex. They may underlie either similarities or differences in brain and behavior of males and females. Some of these genes are autosomal. Others are located on the non-recombining part of the Y chromosome. Genes on this region of the Y chromosome may contribute to sex differences in brain and behavior in three ways. First, a gene may be on the Y chromosome and not on any other chromosome. Thus, it acts only in males. Sex-determining region on the Y chromosome (Sry) is such a gene. Second, there may be different isoforms of proteins coded for by the gene on the Y chromosome and by its homologue located elsewhere in the genome. Such a gene is Smcy which codes for an H-Y antigen. Smcx is its X-chromosomal homologue. Third, there may be different protein levels in males and females for a gene located on the X and Y chromosomes. Zfy and Zfx, for the zinc finger proteins on the Y and on the X, are a pair of such genes. Due to X inactivation in females, one copy of Zfx is expressed in all tissues of female mice, whereas two copies, one of Zfx and one of Zfy, are expressed in many tissues of male mice.Biomedical Reviews 1997; 7: 85-90

A Stable Cranial Neural Crest Cell Line from Mouse

Cranial neural crest cells give rise to ectomesenchymal derivatives such as cranial bones, cartilage, smooth muscle, dentin, as well as melanocytes, corneal endothelial cells, and neurons and glial cells of the peripheral nervous system. Previous studies have suggested that although multipotent stem-like cells may exist during the course of cranial neural crest development, they are transient, undergoing lineage restriction early in embryonic development. We have developed culture conditions that allow cranial neural crest cells to be grown as multipotent stem-like cells. With these methods, we obtained 2 independent cell lines, O9-1 and i10-1, which were derived from mass cultures of Wnt1-Cre; R26R-GFP-expressing cells. These cell lines can be propagated and passaged indefinitely, and can differentiate into osteoblasts, chondrocytes, smooth muscle cells, and glial cells. Whole-genome expression profiling of O9-1 cells revealed that this line stably expresses stem cell markers (CD44, Sca-1, and Bmi1) and neural crest markers (AP-2α, Twist1, Sox9, Myc, Ets1, Dlx1, Dlx2, Crabp1, Epha2, and Itgb1). O9-1 cells are capable of contributing to cranial mesenchymal (osteoblast and smooth muscle) neural crest fates when injected into E13.5 mouse cranial tissue explants and chicken embryos. These results suggest that O9-1 cells represent multipotent mesenchymal cranial neural crest cells. The O9-1 cell line should serve as a useful tool for investigating the molecular properties of differentiating cranial neural crest cells

Mississippi State University Research / Demonstration Module

A final report on the Mississippi State Module Planning Grant prepared by E. T. Kohler and R. C. Maxson in September of 1968

Cyclic dermal BMP signalling regulates stem cell activation during hair regeneration

In the age of stem cell engineering it is critical to understand how stem cell activity is regulated during regeneration. Hairs are mini-organs that undergo cyclic regeneration throughout adult life1, and are an important model for organ regeneration. Hair stem cells located in the follicle bulge2 are regulated by the surrounding microenvironment, or niche3. The activation of such stem cells is cyclic, involving periodic -catenin activity4, 5, 6, 7. In the adult mouse, regeneration occurs in waves in a follicle population, implying coordination among adjacent follicles and the extrafollicular environment. Here we show that unexpected periodic expression of bone morphogenetic protein 2 (Bmp2) and Bmp4 in the dermis regulates this process. This BMP cycle is out of phase with the WNT/-catenin cycle, thus dividing the conventional telogen into new functional phases: one refractory and the other competent for hair regeneration, characterized by high and low BMP signalling, respectively. Overexpression of noggin, a BMP antagonist, in mouse skin resulted in a markedly shortened refractory phase and faster propagation of the regenerative wave. Transplantation of skin from this mutant onto a wild-type host showed that follicles in donor and host can affect their cycling behaviours mutually, with the outcome depending on the equilibrium of BMP activity in the dermis. Administration of BMP4 protein caused the competent region to become refractory. These results show that BMPs may be the long-sought 'chalone' inhibitors of hair growth postulated by classical experiments. Taken together, results presented in this study provide an example of hierarchical regulation of local organ stem cell homeostasis by the inter-organ macroenvironment. The expression of Bmp2 in subcutaneous adipocytes indicates physiological integration between these two thermo-regulatory organs. Our findings have practical importance for studies using mouse skin as a model for carcinogenesis, intra-cutaneous drug delivery and stem cell engineering studies, because they highlight the acute need to differentiate supportive versus inhibitory regions in the host skin

The Legionella effector WipB is a translocated Ser/Thr phosphatase that targets the host lysosomal nutrient sensing machinery

Legionella pneumophila infects human alveolar macrophages and is responsible for Legionnaire’s disease, a severe form of pneumonia. L. pneumophila encodes more than 300 putative effectors, which are translocated into the host cell via the Dot/Icm type IV secretion system. These effectors highjack the host’s cellular processes to allow bacterial intracellular growth and replication. Here we adopted a multidisciplinary approach to investigate WipB, a Dot/Icm effector of unknown function. The crystal structure of the N-terminal domain at 1.7 Å resolution comprising residues 25 to 344 revealed that WipB harbours a Ser/Thr phosphatase domain related to the eukaryotic phospho-protein phosphatase (PPP) family. The C-terminal domain (residues 365–524) is sufficient to pilot the effector to acidified LAMP1-positive lysosomal compartments, where WipB interacts with the v-ATPase and the associated LAMTOR1 phosphoprotein, key components of the lysosomal nutrient sensing (LYNUS) apparatus that controls the mammalian target of rapamycin (mTORC1) kinase complex at the lysosomal surface. We propose that WipB is a lysosome-targeted phosphatase that modulates cellular nutrient sensing and the control of energy metabolism during Legionella infection

The Role of Paracrine and Autocrine Signaling in the Early Phase of Adipogenic Differentiation of Adipose-derived Stem Cells.

INTRODUCTION: High cell density is known to enhance adipogenic differentiation of mesenchymal stem cells, suggesting secretion of signaling factors or cell-contact-mediated signaling. By employing microfluidic biochip technology, we have been able to separate these two processes and study the secretion pathways. METHODS AND RESULTS: Adipogenic differentiation of human adipose-derived stem cells (ASCs) cultured in a microfluidic system was investigated under perfusion conditions with an adipogenic medium or an adipogenic medium supplemented with supernatant from differentiating ASCs (conditioned medium). Conditioned medium increased adipogenic differentiation compared to adipogenic medium with respect to accumulation of lipid-filled vacuoles and gene expression of key adipogenic markers (C/EBPα, C/EBPβ, C/EBPδ, PPARγ, LPL and adiponectin). The positive effects of conditioned medium were observed early in the differentiation process. CONCLUSIONS: Using different cell densities and microfluidic perfusion cell cultures to suppress the effects of cell-released factors, we have demonstrated the significant role played by auto- or paracrine signaling in adipocyte differentiation. The cell-released factor(s) were shown to act in the recruitment phase of the differentiation process

Cadmium levels in a North Carolina cohort: Identifying risk factors for elevated levels during pregnancy

The objectives of this study were to examine cadmium (Cd) levels and relationships to demographics in an observational, prospective pregnancy cohort study in Durham County, North Carolina. Multivariable models were used to compare blood Cd levels across demographic characteristics. The relative risk of having a blood Cd level that exceeds the US national median (0.32 μg/l) was estimated. Overall, >60% of the women had an elevated (>0.32 μg/l) blood Cd level. Controlling for confounding variables, smoking was associated with 21% (95% CI: 15–28%) increased risk for an elevated blood Cd level. High Cd levels were also observed in non-smokers and motivated smoking status-stratified models. Race, age, education, relationship status, insurance status and cotinine level were not associated with risk of elevated Cd levels among smokers; however, older age and higher cotinine levels were associated with elevated Cd levels among non-smokers. Taken together, more than half of pregnant women in this cohort had elevated blood Cd levels. Additionally, among non-smokers, 53% of the women had elevated levels of Cd, highlighting other potential sources of exposure. This study expands on the limited data describing Cd levels in pregnant populations and highlights the importance of understanding Cd exposures among non-smokers. Given the latent health risks of both smoking and Cd exposure, this study further highlights the need to biomonitor for exposure to toxic metals during pregnancy among all women of child-bearing age

Medical treatment of prolactinomas.

Prolactinomas, the most prevalent type of neuroendocrine disease, account for approximately 40% of all pituitary adenomas. The most important clinical problems associated with prolactinomas are hypogonadism, infertility and hyposexuality. In patients with macroprolactinomas, mass effects, including visual field defects, headaches and neurological disturbances, can also occur. The objectives of therapy are normalization of prolactin levels, to restore eugonadism, and reduction of tumor mass, both of which can be achieved in the majority of patients by treatment with dopamine agonists. Given their association with minimal morbidity, these drugs currently represent the mainstay of treatment for prolactinomas. Novel data indicate that these agents can be successfully withdrawn in a subset of patients after normalization of prolactin levels and tumor disappearance, which suggests the possibility that medical therapy may not be required throughout life. Nevertheless, multimodal therapy that involves surgery, radiotherapy or both may be necessary in some cases, such as patients who are resistant to the effects of dopamine agonists or for those with atypical prolactinomas. This Review reports on efficacy and safety of pharmacotherapy in patients with prolactinomas